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Original Articles
- Effects of Exposure to Hexavalent Chromium on the Level of 8-Hydroxydeoxyguanosine and the Activities of Superoxide Dismutase and 8-Hydroxyguanine Endonuclease in Rat Lung .
- Heon Kim, Hun Sik Kim, Rosa Kim, Hyeon Yeong Kim, Jae Hwang Jeong
- Korean J Prev Med. 1999;32(1):101-107.
- 1,848 View
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Abstract
PDF - OBJECTIVES
To determine the effects of exposure to hexavalent chromium, 93 male Sprague-Dawley rats were exposed to hexavalent chromium solution. METHODS: Rats were divided into 4 groups and exposed to 0.1 ml of 0 mM, 0.4 mM, 2.0 mM, and 10.0 mM potassium chromate in the first experiment, and to 0.1 ml of 0 mM, 20 mM, 40 mM, and 80 mM in the second for consecutive 3 days by tracheal instillation. Three and 10 rats were the controls for the first and the second experiments, respectively. Lung tissues were then removed to measure the 8-hydroxydeoxyguanosine (8-OH-dG) level using the HPLC-ECD method, superoxide dismutase (SOD) activity using the cytochrome C method, and 8-hydroxyguanine endonuclease activity using the oligonucleotide nicking assay. RESULTS: The results showed no significant linear relationship between chromium exposure level and 8-OH-dG level or 8-hydroxyguanine endonuclease activity. In the first experiment, 8-OH-dG level and 8-hydroxyguanine endonuclease activity increased in 0.4 mM group, and then decreased in 2.0 mM and 10.0 mM groups. The correlation coefficients between 8-OH-dG level and 8-hydroxyguanine endonuclease activity was statistically significant (P<0.01), and total SOD activity was elevated by chromium exposure in a dose-dependent manner (P<0.05). In contrast, there was no significant dose-response pattern or correlation in the second experiment. CONCLUSIONS: Based on the fact that there was no linear relationship between chromium dose and 8-OH-dG level or activity of the repair enzyme, it seems unlikely that 8-OH-dG formation is the major mechanism of chromium carcinogenesis. -
SummaryTOP
- The effects of chromium exposure on sister chromatid exchange and concentration of 8-hydroxydeoxyguanosine.
- Sang Hwan Han, Soo Hun Cho, Heon Kim, Soo Min Park, Mina Ha, Young Soo Joo, Ho Jang Kwon, Yong Dae Kwon, Myung Hee Kwon
- Korean J Prev Med. 1995;28(2):511-525.
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Abstract
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- To elucidate some DNA adducts as a biological marker for workers of chromate pigment, the effects of chromium exposure on the formation of 8-hydroxydeoxyguanosine(8-OH-dG) and sister chromatid exchanges(SCEs) frequency in 38 workers of a pigment plant in Bucheon which utilized lead chromates, were examined. The chromium contents of venous blood and urine were measured as working environmental exposure level. The concentrations of 8-OH-dG in DNA isolated from lymphocytes were determined with high performance liquid chromatography and electrochemical detector and denoted as a molar ratio of 8-OH-dG to deoxyguanosine(dG). The SCEs frequency were analyzed in DNA isolated from lymphocytes. A significant correlation was found between creatinine adjusted urine chromium concentration and the molar ratio of 8-OH-dG to dG(r=0.47, p<0.01). After adjusting the current smoking habit, the correlation coefficient was increased(r=0.62, p<0.05). However, there was no significant correlation between the SCE frequency and chromium exposure. This significant results between molar ratio of 8-OH-dG to dG and chromium exposure are in good agreement with in vitro studies that support the importance of DNA adduct formation for the carcinogenic effect of chromium.
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SummaryComparative Study
- Effects of Oxidative DNA Damage and Genetic Polymorphism of the Glutathion Peroxidase 1 (GPX1) and 8-Oxoguanine Glycosylase 1 (hOGG1) on Lung Cancer.
- Chul Ho Lee, Kye Young Lee, Kang Hyeon Choe, Yun Chul Hong, Sung Il Noh, Sang Yong Eom, Young Jun Ko, Yan Wei Zhang, Dong Hyuk Yim, Jong Won Kang, Heon Kim, Yong Dae Kim
- J Prev Med Public Health. 2006;39(2):130-134.
- 2,499 View
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Abstract
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- OBJECTIVES
Oxidative DNA damage is a known risk factor of lung cancer. The glutathione peroxidase (GPX) antioxidant enzyme that reduces hydrogen peroxide and lipid peroxides plays a significant role in protecting cells from the oxidative stress induced by reactive oxygen species. The aim of this case-control study was to investigate effects of oxidative stress and genetic polymorphisms of the GPX1 genes and the interaction between them in the carcinogenesis of lung cancer. METHODS: Two hundreds patients with lung cancer and 200 age- and sex-matched controls were enrolled in this study. Every subject was asked to complete a questionnaire concerning their smoking habits and their environmental exposure to PAHs. The genotypes of the GPX1 and 8-oxoguanine glycosylase 1 (hOGG1) genes were examined and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) were measured. RESULTS: Cigarette smoking was a significant risk factor for lung cancer. The levels of urinary 8-OH-dG were higher in the patients (p<0.001), whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. The GPX1 codon 198 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Pro/Leu or Leu/Leu genotype of GPX1 were at a higher risk for lung cancer (adjusted OR=2.29). In addition, these individuals were shown to have high urinary 8-OH-dG concentrations compared to the individuals with the GPX1 Pro/Pro genotype. On the other hand, the polymorphism of the hOGG1 gene did not affect the lung cancer risk and the oxidative DNA damage. CONCLUSIONS: These results lead to a conclusion that individuals with the GPX1 Pro/Leu or Leu/Leu genotype would be more susceptible to the lung cancer induced by oxidative stress than those individuals with the Pro/Pro genotype. -
SummaryEnglish Abstract
- Effects of Oxidative DNA Damage Induced by Polycyclic Aromatic Hydrocarbons and Genetic Polymorphism of the Paraoxonase-1 (PON1) Gene on Lung Cancer.
- Chul Ho Lee, Kye Young Lee, Kang Hyeon Choe, Yun Chul Hong, Yong Dae Kim, Jong Won Kang, Heon Kim
- J Prev Med Public Health. 2005;38(3):345-350.
- 2,664 View
- 80 Download
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Abstract
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- OBJECTIVE
Polycyclic aromatic hydrocarbons (PAHs), which are risk factors for lung cancer, have been reported to induce oxidative DNA damage. The paraoxonase (PON) plays a significant role in the detoxification of a variety of organophosphorous compounds, with paraoxonase-1 (PON1) being one of the endogenous free-radical scavenging systems in the human body. The aim of this case-control study was to investigate the effects of PAH exposure, oxidative stress and the Q192R polymorphism of PON1 genes, and their interactions in the carcinogenesis of lung cancer. METHODS: One hundred and seventy seven lung cancer patients and 177 age- and sex-matched controls were enrolled in this study. Each subject was asked to complete a questionnaire concerning their smoking habits and environmental exposure to PAHs. The Q192R genotypes of the PON1 gene was examined, and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8- hydroxydeoxyguanosine (8-OH-dG) measured. RESULTS: Cigarette smoking was found to be a significant risk factor for lung cancer. The urinary 8-OH-dG level was higher in the patients, whereas the urinary 1-OHP and 2- naphthol levels were higher in the controls. There was a significant correlation between the urinary levels of 8-OHdG and 1-OHP in both the cases and controls. The PON1 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Q/Q genotype of the PON1 gene were found to be at higher risk of developing lung cancer. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in those with the PON1 Q/Q genotype. CONCLUSIONS: These results lead to the conclusion that PAHs would induce oxidative DNA damage, especially in individuals with the PON1 Q/Q genotype. Therefore, people with the PON1 Q/Q genotype would be more susceptible to lung cancer than those with the R/R or Q/R genotypes of the PON1 gene. -
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